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Chemistry

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Also known as: G-strophanthin, Ouabaine, Acocantherin, Ouabagenin l-rhamnoside, Oubain, Purostrophan
Molecular Formula
C29H44O12
Molecular Weight
584.7  g/mol
InChI Key
LPMXVESGRSUGHW-HBYQJFLCSA-N
FDA UNII
5ACL011P69

Ouabain
A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like DIGITALIS. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-EXCHANGING ATPASE.
1 2D Structure

Ouabain

2 Identification
2.1 Computed Descriptors
2.1.1 IUPAC Name
3-[(1R,3S,5S,8R,9S,10R,11R,13R,14S,17R)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxy-2,3,4,6,7,8,9,11,12,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-17-yl]-2H-furan-5-one
2.1.2 InChI
InChI=1S/C29H44O12/c1-13-22(34)23(35)24(36)25(40-13)41-15-8-19(32)28(12-30)21-17(3-5-27(28,37)9-15)29(38)6-4-16(14-7-20(33)39-11-14)26(29,2)10-18(21)31/h7,13,15-19,21-25,30-32,34-38H,3-6,8-12H2,1-2H3/t13-,15-,16+,17+,18+,19+,21+,22-,23+,24+,25-,26+,27-,28+,29-/m0/s1
2.1.3 InChI Key
LPMXVESGRSUGHW-HBYQJFLCSA-N
2.1.4 Canonical SMILES
CC1C(C(C(C(O1)OC2CC(C3(C4C(CCC3(C2)O)C5(CCC(C5(CC4O)C)C6=CC(=O)OC6)O)CO)O)O)O)O
2.1.5 Isomeric SMILES
C[C@H]1[C@@H]([C@H]([C@H]([C@@H](O1)O[C@H]2C[C@H]([C@@]3([C@@H]4[C@@H](CC[C@@]3(C2)O)[C@]5(CC[C@@H]([C@]5(C[C@H]4O)C)C6=CC(=O)OC6)O)CO)O)O)O)O
2.2 Other Identifiers
2.2.1 UNII
5ACL011P69
2.3 Synonyms
2.3.1 MeSH Synonyms

1. Acocantherin

2. Acolongifloroside K

3. G Strophanthin

4. G-strophanthin

2.3.2 Depositor-Supplied Synonyms

1. G-strophanthin

2. Ouabaine

3. Acocantherin

4. Ouabagenin L-rhamnoside

5. Oubain

6. Purostrophan

7. Ouabain Anhydrous

8. Gratus Strophanthin

9. Strodival

10. Astrobain

11. Gratibain

12. Ouabain Octahydrate

13. 630-60-4

14. Strophoperm

15. Acocantherine

16. Ouabagenin-l-rhamnosid

17. Strophalen

18. Kombetin

19. Uabaina

20. Rectobaina

21. Solufantina

22. Strophosan

23. G-strophicor

24. Chebi:472805

25. G-strophanthin (jan)

26. Uabanin

27. Mls000069786

28. Chembl222863

29. Nsc-25485

30. 5acl011p69

31. Strophantin-g

32. Quabain

33. Smr000058492

34. Strophanthin-g

35. Dsstox_cid_23765

36. Dsstox_rid_80072

37. Dsstox_gsid_43765

38. G-strophanthin [jan]

39. 3-(alpha-l-rhamnopyranosyloxy)-1beta,5beta,11alpha,14,19-pentahydroxy-5beta-card-20(22)-enolide

40. Card-20(22)-enolide, 3-[(6-deoxy-.alpha.-l-mannopyranosyl)oxy]-1,5,11,14,19-pentahydroxy-, (1.beta.,3.beta.,5.beta.,11.alpha.)-

41. Obn

42. Ouabain, Octahydrate

43. Cardiac Glycoside

44. 4-[(1s,2r,3r,5s,7s,10r,11s,14r,15r,17r)-3,7,11,17-tetrahydroxy-2-(hydroxymethyl)-15-methyl-5-{[(2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxy}tetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadecan-14-yl]-2,5-dihydrofuran-2-one

45. Cas-630-60-4

46. Ouabagenin-l-rhamnosid [german]

47. Sr-01000076047

48. Ccris 965

49. Unii-5acl011p69

50. Hsdb 3519

51. 1ibg

52. Ncgc00163473-01

53. 3-[(1r,3s,5s,8r,9s,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-[(2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyl-tetrahydropyran-2-yl]oxy-2,3,4,6,7,8,9,11,12,15,16,17-dodecahydro-1h-cyclopenta[a]phenanthren-17-yl]-2h-furan-5-one

54. Card-20(22)-enolide, 3-((6-deoxy-.alpha.-l-mannopyranosyl)oxy)-1,5,11,14,19-pentahydroxy-, (1.beta.,3.beta.,5.beta.,11.alpha.)-

55. Einecs 211-139-3

56. Nsc 25485

57. Brn 0101712

58. 3a3y

59. Opera_id_395

60. Ouabain [mi]

61. Ouabain [mart.]

62. Prestwick0_000471

63. Prestwick1_000471

64. Prestwick2_000471

65. Prestwick3_000471

66. Ouabain [who-dd]

67. Epitope Id:161502

68. O 3125

69. G-strophanthin [mi]

70. Lopac0_000943

71. Schembl15433

72. Bspbio_000602

73. 5-18-05-00625 (beilstein Handbook Reference)

74. Card-20(22)-enolide, 3-((6-deoxy-alpha-l-mannopyranosyl)oxy)-1,5,11,14,19-pentahydroxy-, (1beta,3beta,5beta,11alpha)-

75. Spbio_002541

76. Ouabain [ep Monograph]

77. Bpbio1_000664

78. Cid_439501

79. Gtpl4826

80. Dtxsid0043765

81. Ouabain Anhydrous [hsdb]

82. Regid_for_cid_439501

83. 3n23

84. Hms2089j19

85. Hms2235a07

86. Hms3262n08

87. Zinc8143614

88. Tox21_110024

89. Tox21_112057

90. Tox21_301547

91. Tox21_500943

92. Bdbm50286739

93. Akos024285581

94. Tox21_112057_1

95. Ccg-205024

96. Ccg-208243

97. Db01092

98. Lp00943

99. Sdccgsbi-0050917.p002

100. 3-((6-deoxy-alpha-l-mannopyranosyl)oxy)-1,5,11alpha,14,19-pentahydroxycard-20(22)-enolide

101. 3-(6-deoxy-alpha-l-mannopyranosyloxy)-1,5,11a,14,19-pentahydroxycard-20(22)-enolide

102. Smp1_000142

103. Ncgc00013319-01

104. Ncgc00015769-17

105. Ncgc00015769-32

106. Ncgc00017394-02

107. Ncgc00017394-07

108. Ncgc00017394-11

109. Ncgc00255970-01

110. Ncgc00261628-01

111. Ncgc00263656-01

112. Eu-0100943

113. C01443

114. D00112

115. Q285911

116. Sr-01000721848

117. Sr-01000076047-1

118. Sr-01000076047-5

119. Sr-01000721848-2

120. Sr-01000721848-4

121. Brd-k35708212-331-03-1

122. (1.beta.,3.beta.,5.beta.,11.alpha.)-3-((6-deoxy-.alpha.-l-mannopyranosyl)oxy)-1,5,11,14,19-pentahydroxycard-20(22)-enolide

123. (1alpha,3beta,5beta,11alpha,17alpha)-3-[(6-deoxy-alpha-l-mannopyranosyl)oxy]-1,5,11,14,19-pentahydroxycard-20(22)-enolide

124. 3-[(6-deoxy-.alpha.-l-mannopyranosyl)oxy]-1,5,11.alpha.,14,19-pentahydroxycard-20(22)-enolide

125. 4-((1r,3s,5s,8r,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-((2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyl-tetrahydro-2h-pyran-2-yloxy)-hexadecahydro-1h-cyclopenta[a]phenanthren-17-yl)furan-2(5h)-one

126. 4-((1r,3s,5s,8r,9s,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-(((2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyltetrahydro-2h-pyran-2-yl)oxy)hexadecahydro-1h-cyclopenta[a]phenanthren-17-yl)furan-2(5h)-one

127. 4-((1r,3s,5s,8r,9s,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-((2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyl-tetrahydro-2h-pyran-2-yloxy)-hexadecahydro-1h-cyclopenta[a]phenanthren-17-yl)furan-2(5h)-one

128. 4-((1r,3s,5s,9s,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-(hydroxymethyl)-13-methyl-3-((2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyltetrahydro-2h-pyran-2-yloxy)hexadecahydro-1h-cyclopenta[a]phenanthren-17-yl)furan-2(5h)-one

129. 4-[(1r,3s,5s,10r,11r,13r,14s,17r)-1,5,11,14-tetrahydroxy-10-hydroxymethyl-13-methyl-3-((2r,3r,4r,5r,6s)-3,4,5-trihydroxy-6-methyl-tetrahydro-pyran-2-yloxy)-hexadecahydro-cyclopenta[a]phenanthren-17-yl]-5h-furan-2-one

130. 4-[(r)-1,5,11,14-tetrahydroxy-10-hydroxymethyl-13-methyl-3-(3,4,5-trihydroxy-6-methyl-tetrahydro-pyran-2-yloxy)-hexadecahydro-cyclopenta[a]phenanthren-17-yl]-5h-furan-2-one

131. 4-[1,5,11,14-tetrahydroxy-10-hydroxymethyl-13-methyl-3-(3,4,5-trihydroxy-6-methyl-tetrahydro-pyran-2-yloxy)-hexadecahydro-cyclopenta[a]phenanthren-17-yl]-5h-furan-2-one

132. 4-[1,5,11,14-tetrahydroxy-10-hydroxymethyl-13-methyl-3-(3,4,5-trihydroxy-6-methyl-tetrahydro-pyran-2-yloxy)-hexadecahydro-cyclopenta[a]phenanthren-17-yl]-5h-furan-2-one(ouabain)

133. Ouabain4-[1,5,11,14-tetrahydroxy-10-hydroxymethyl-13-methyl-3-(3,4,5-trihydroxy-6-methyl-tetrahydro-pyran-2-yloxy)-hexadecahydro-cyclopenta[a]phenanthren-17-yl]-5h-furan-2-one

2.4 Create Date
2005-06-24
3 Chemical and Physical Properties
Molecular Weight 584.7 g/mol
Molecular Formula C29H44O12
XLogP3-1.7
Hydrogen Bond Donor Count8
Hydrogen Bond Acceptor Count12
Rotatable Bond Count4
Exact Mass584.28327683 g/mol
Monoisotopic Mass584.28327683 g/mol
Topological Polar Surface Area207 Ų
Heavy Atom Count41
Formal Charge0
Complexity1080
Isotope Atom Count0
Defined Atom Stereocenter Count15
Undefined Atom Stereocenter Count0
Defined Bond Stereocenter Count0
Undefined Bond Stereocenter Count0
Covalently Bonded Unit Count1
4 Drug and Medication Information
4.1 Therapeutic Uses

/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Ouabain is included in the database.

NIH/NLM; ClinicalTrials.Gov. Available from, as of February 1, 2017: https://clinicaltrials.gov/ct2/results?term=Ouabain&Search=Search


/EXPL THER/ Up-regulation of placental soluble fms-like tyrosine kinase 1 (sFlt1) contributes to the pathogenesis of preeclampsia. To evaluate novel upstream pathways that regulate placental sFlt1 production, we screened a library of natural compounds (n=502) in human placental cell lines. Here, we report 3 compounds in the cardiac glycoside family, ouabain, gitoxigenin, and digitoxin, that inhibit placental sFlt1 production at nanomolar concentrations in vitro. We further characterized ouabain and demonstrated that it inhibits sFlt1 mRNA and protein expression in human placental cytotrophoblasts and explant cultures in a dose- and time-dependent manner. Ouabain down-regulated sFlt1 production by inhibiting hypoxia-inducible factor 1 (HIF-1alpha) protein expression in the placenta. Furthermore, we found that phosphorylation of heat-shock protein 27 (HSP27) was necessary for ouabain to inhibit HIF-1alpha translation. In a rat model of pregnancy-induced hypertension, ouabain reduced mean arterial pressure and enhanced placental HSP27 phosphorylation without any adverse effects on pups ...

PMID:24970393 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202104 Rana S et al; FASEB J 28 (10): 4324-34 (2014)


/EXPL THER/ Cytotoxicity and proliferative effects of ouabain on H460 lung cancer cells were evaluated by the MTT assay. The levels of integrin proteins in response to ouabain were determined by western blotting. Anchorage-independent growth and migration behaviors were performed by the wound healing assay and colony formation assay, respectively. Herein, the results suggested that exposure of the lung cancer cells to physiological concentrations of ouabain significantly altered the level of integrins. Ouabain suppressed integrin alpha-4, alpha-5, alpha-v, beta-3 and beta-4, whereas it had no significant effect on integrin beta-1 and beta-4. According to the switch patterns of integrins, ouabain treatment resulted in a dramatic reduction of cell colony size and inhibition of cancer cell migration. However, ouabain-induced integrin switch had only a slight effect on chemotherapeutic drug susceptibility. Ouabain may have a role in suppressing cancer metastasis via integrin regulation.

PMID:25275046 Ninsontia C, Chanvorachote P; Anticancer Res 34 (10): 5495-502 (2014)


A recent study confirmed the long-known clinical experience that ouabain has an inhibitory effect on cardiotoxicity induced by digitalis glycosides. Ouabain at a low dosage delayed the start of arrythmia induced by digoxin on guinea pig papillary muscle. In addition, ouabain at a low dosage but not at a high dosage delayed the development of digoxin-induced arrhythmia in anesthetized guinea pigs. Thus, the long-known characteristic dose dependency of ouabain effects has been confirmed.

Furstenwerth H; lnt J Clin Pract 64 (12) 1591-4 (2010)


For more Therapeutic Uses (Complete) data for Ouabain (11 total), please visit the HSDB record page.


4.2 Drug Indication

For the treatment of atrial fibrillation and flutter and heart failure


5 Pharmacology and Biochemistry
5.1 Pharmacology

Ouabain, a cardiac glycoside similar to digitoxin, is used to treat congestive heart failure and supraventricular arrhythmias due to reentry mechanisms, and to control ventricular rate in the treatment of chronic atrial fibrillation.


5.2 MeSH Pharmacological Classification

Enzyme Inhibitors

Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)


Cardiotonic Agents

Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE). (See all compounds classified as Cardiotonic Agents.)


5.3 ATC Code

C - Cardiovascular system

C01 - Cardiac therapy

C01A - Cardiac glycosides

C01AC - Strophanthus glycosides

C01AC01 - G-strophanthin


5.4 Absorption, Distribution and Excretion

The effect of i.v.-administered ouabain starts immediately after injection, reaches a maximum after 5 min, last 5-7 hr and then rapidly declines.

Furstenwerth H; lnt J Clin Pract 64 (12) 1591-4 (2010)


It is poorly absorbed from alimentary tract, where much of oral dose appears to be destroyed.

Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-842


Four, 7 and 10% of (3)H-ouabain had been absorbed 1, 5 and 15 hr respectively after oral administration to guinea pigs. Percentage absorbed was constant at each of 3 dose levels. ... Similar results obtained in man. ... /It/ was absorbed from GI tract of rats by passive diffusion. Absorption of im dose probably depended more on tissue-blood flow than on rates of diffusion ... 67% of iv dose was excreted in 30-min bile of rats. ... /It/ was actively transported from liver to bile, and carbon tetrachloride pretreatment of rats reduced biliary excretion by depressing this transport.

The Chemical Society. Foreign Compound Metabolism in Mammals. Volume 2: A Review of the Literature Published Between 1970 and 1971. London: The Chemical Society, 1972., p. 67


Plasma clearance of ouabain following iv admin was much faster in rat than in rabbit or dog. Levels of radioactivity in plasma, bile, and liver ... determined 20 min after iv administration ... showed that rat exhibited overall bile to plasma concentration ratio of 1500, whereas same ratio was much less for rabbit (2.9) and dog (9.3). Liver/plasma and bile/liver concentration ratios ... were ... much greater in rat (20 and 71) than in rabbit (2.5 and 1.3) or dog (3.3 and 2.7). This species variation is thought to be important factor in resistance of rat to toxic effects of ouabain relative to rabbit and dog.

The Chemical Society. Foreign Compound Metabolism in Mammals Volume 3. London: The Chemical Society, 1975., p. 575


For more Absorption, Distribution and Excretion (Complete) data for Ouabain (7 total), please visit the HSDB record page.


5.5 Metabolism/Metabolites

Ouabain ... is not bound extensively to plasma albumin and ... /is/ excreted largely unchanged.

Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975., p. 673


5.6 Biological Half-Life

... Almost entirely eliminated by renal excretion, with a biological-half-life ... about 21 hr in normal adults but longer in elderly persons & much longer in renal failure.

Osol, A. (ed.). Remington's Pharmaceutical Sciences. 16th ed. Easton, Pennsylvania: Mack Publishing Co., 1980., p. 798


5.7 Mechanism of Action

Ouabain inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium and calcium concentrations. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Ouabain also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.


Ouabain, an endogenous digitalis compound, has been detected in nanomolar concentrations in the plasma of several mammals and is associated with the development of hypertension. In addition, plasma ouabain is increased in several hypertension models, and the acute or chronic administration of ouabain increases blood pressure in rodents. These results suggest a possible association between ouabain and the genesis or development and maintenance of arterial hypertension. One explanation for this association is that ouabain binds to the alpha-subunit of the Na(+) pump, inhibiting its activity. Inhibition of this pump increases intracellular Na(+), which reduces the activity of the sarcolemmal Na(+)/Ca(2+) exchanger and thereby reduces Ca(2+) extrusion. Consequently, intracellular Ca(2+) increases and is taken up by the sarcoplasmic reticulum, which, upon activation, releases more calcium and increases the vascular smooth muscle tone. In fact, acute treatment with ouabain enhances the vascular reactivity to vasopressor agents, increases the release of norepinephrine from the perivascular adrenergic nerve endings and promotes increases in the activity of endothelial angiotensin-converting enzyme and the local synthesis of angiotensin II in the tail vascular bed. Additionally, the hypertension induced by ouabain has been associated with central mechanisms that increase sympathetic tone, subsequent to the activation of the cerebral renin-angiotensin system. Thus, the association with peripheral mechanisms and central mechanisms, mainly involving the renin-angiotensin system, may contribute to the acute effects of ouabain-induced elevation of arterial blood pressure.

PMID:21956536 Padilha AS et al; Braz J Med Biol Res 44 (9): 933-8 (2011)


The migratory capability of cancer cells is one of the most important hallmarks reflecting metastatic potential. Ouabain, an endogenous cardiac glycoside produced by the adrenal gland, has been previously reported to have anti-tumor activities; however, its role in the regulation of cancer cell migration remains unknown. The present study has revealed that treatment with ouabain at physiological concentrations is able to inhibit the migratory activities of human lung cancer H292 cells. The negative effects of ouabain were found to be mediated through the suppression of migration regulatory proteins, such as focal adhesion kinase (FAK), ATP-dependent tyrosine kinase (Akt), and cell division cycle 42 (Cdc42). We found that the observed actions of ouabain were mediated via a reactive oxygen species (ROS)-dependent mechanism because the addition of ROS scavengers (N-acetylcysteine and glutathione) could reverse the effect of ouabain on cell migration. Furthermore, ouabain was shown to inhibit the spheroidal tumor growth and decrease the cancer cell adhesion to endothelial cells. However, the compound had no significant effect on anoikis of the cells. ...

PMID:23874694 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3707866 Pongrakhananon V et al; PLoS One 8 (7): e68623 (2013)


The steroid Na(+)/K(+) ATPase (NKA) blocker ouabain has been shown to exhibit pro-apoptotic effects in various cell systems; however, the mechanism involved in those effects is unclear. Here, we have demonstrated that incubation of HeLa cells during 24 hr with nanomolar concentrations of ouabain or digoxin causes apoptotic death of 30-50% of the cells. Ouabain caused the activation of caspases-3/7 and -9; however, caspase-8 was unaffected. The fact that compound Z-LEHD-FMK reduced both apoptosis and caspase-9 activation elicited by ouabain, suggest a mitochondrially-mediated pathway. This was strengthened by the fact that ouabain caused ATP depletion and the release of mitochondrial cytochrome c into the cytosol. Furthermore, upon ouabain treatment mitochondrial disruption and redistribution into the cytosol were observed. A mitochondrial site of action for ouabain was further corroborated by tight co-localization of fluorescent ouabain with mitochondria. Finally, in ouabain-treated cells the histamine-elicited elevation of cytosolic Ca(2+) concentration ([Ca(2+)]c) suggests an additional effect on the endoplasmic reticulum (ER) leading to Ca(2+) store depletion. We conclude that fluorescent ouabain is taken up and tightly co-localizes with mitochondria of HeLa cells. This indicates that apoptosis may be triggered by a direct action of ouabain on mitochondria.

PMID:23933121 Alonso E et al; Steroids 78 (11): 1110-8 (2013)


Ouabain, a potent inhibitor of the Na(+), K(+)-ATPase, was identified as an endogenous substance. Recently, ouabain was shown to affect various immunological processes. We have previously demonstrated the ability of ouabain to modulate inflammation, but little is known about the mechanisms involved. Thus, the aim of the present work is to evaluate the immune modulatory role of ouabain on zymosan-induced peritonitis in mice. Our results show that ouabain decreased plasma exudation (33%). After induction of inflammation, OUA treatment led to a 46% reduction in the total number of cells, as a reflex of a decrease of polymorphonuclear leukocytes, which does not appear to be due to cell death. Furthermore, OUA decreased TNF-alpha (57%) and IL-1beta (58%) levels, without interfering with IL-6 and IL-10. Also, in vitro experiments show that ouabain did not affect endocytic capacity. Moreover, electrophoretic mobility shift assay (EMSA) shows that zymosan treatment increased (85%) NF-kappaB binding activity and that ouabain reduced (30%) NF-kappaB binding activity induced by zymosan. Therefore, our data suggest that ouabain modulated acute inflammatory response, reducing the number of cells and cytokines levels in the peritoneal cavity, as well as NFkappaB activation, suggesting a new mode of action of this substance.

PMID:26078492 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4442290 Leite JA et al; Mediators Inflamm 2015: 265798 doi: 10.1155/2015/265798 (2015)


For more Mechanism of Action (Complete) data for Ouabain (9 total), please visit the HSDB record page.


REF. STANDARDS & IMPURITIES

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